Racemic oxybutynin (OXY) is used therapeutically in the treatment of urinary incontinence due to detrusor muscle instability. OXY exerts a spasmolytic effect by inhibiting the receptors for acetylcholine on smooth muscle. OXY is selective for muscarinic acetylcholine receptors over nicotinic receptors and as a result, no blocking effects are observed at skeletal neuromuscular junctions.
In patients with conditions characterized by involuntary bladder contractions, clinical studies have demonstrated that OXY increases bladder capacity, diminishes the frequency of involuntary contractions of the detrusor muscle, and delays the initial desire to void. OXY is therefore useful in the treatment and prevention of both incontinency and frequent voluntary urination. Antimuscarinic side effects of OXY, such as mydriasis, xerostomia and tachycardia, cannot be avoided with this drug since therapeutic anticholinergic effects are sought [Lish et al. Arch. Int. Pharmacodyn. 156, 467-488 (1965), 481].
Racemic oxybutynin consists of a 50/50 mixture of R(-)-oxybutynin and S(+)-oxybutynin. It has been shown that practically all of the anticholinergic activity of OXY resides in the R(-)-isomer, and the S(+)-isomer carries only a small fraction of the drug's anticholinergic activity (Noronha-Blob et al., J. Pharmacol. Exp. Ther., 1991, 256: 562-567). However, it has now been shown that more serious toxicological activities of oxybutynin express cardiovascular depression and possibly also respiratory depression.
One clinically important metabolite of OXY has been identified in humans after administration of OXY and is called desethyloxybutynin (DEO) (Westlin, L., 1985. Internal report, Smith & Nephew Pharmaceuticals Ltd.). A second metabolite, called N-oxide-oxybutynin, has been suggested but may not be chemically stable (Lindeke B. et al., 1981 Metabolism of Oxybutynin . . . Biomed Mass Spectrometry. 1981, 8:506-513).